The human body contains a number of organs or organ components, both solid and tubular, having a hollow interior. Examples of hollow or tubular organs or organ components include the heart and arteries, the stomach, small and large intestines, bladder, lungs, etc. During the course of a lifetime, the function of these organ or organ components may change, including loss of function (“hypo-normal function”), enhancement of function (“hyper-” or “supra-normal function”) or the attainment or “re-attainment” of normal functions. Hypo-normal function may develop due to atrophy, toxemia, environmental exposure, infection, inflammation, malignancy, injury, ischemia, malnutrition, radiation exposure, temperature alteration, infiltrative processes, fibrotic processes, calcification, lipid insulation, atherosclerosis, and/or physical and/or mechanical stressors. Hyper-normal function may develop due to hyperplasia, hypertrophy, different types of stimulation, including nutritional, metabolic, and/or supplement-stimulation, cellular infiltrative processes, exposure to a number of factors, including environment, radiation, hormones, temperature and/or pharmacological exposure, hyperemia, hyper- or super-fusion, malignancy, physical and/or mechanical stressors, and/or tissue implantation or transplantation.
An example of problems that occur in hollow organs can be seen looking at the coronary arteries. Coronary arteries, or arteries of the heart, perfuse the cardiac muscle with arterial blood. They also provide essential nutrients, removal of metabolic wastes, and gas exchange. These arteries are subject to relentless service demands for continuous blood flow throughout the life of the patient. Despite their critical life supporting function, coronary arteries are often subject to attack through several disease processes, the most notable being atherosclerosis (hardening of the arteries). Throughout the life of the patient, multiple factors contribute to the development of microscopic and/or macroscopic vascular lesions, known as plaques. The development of a plaque-lined vessel typically leads to an irregular inner vascular surface with a corresponding reduction of lumen cross-sectional area. The progressive reduction in cross-sectional area compromises flow through the vessel. In the case of the coronary arteries, the result is a reduction in blood flow to the cardiac muscle. This reduction in blood flow, coupled with a corresponding reduction in nutrient and oxygen supply, often results in clinical angina, unstable angina, myocardial infarction (heart attack), and death. The clinical consequences of the above process and its overall importance are evidenced by the fact that atherosclerotic coronary artery disease is a leading cause of death in the United States.
In 1987, a mechanical approach to combat atherosclerosis and restenosis was introduced. An intracoronary stent is a tubular device made of fine wire mesh, typically stainless steel. A stent of that type is disclosed in U.S. Pat. No. 4,655,771 to Hans Wallsten. The device can be radially compressed so as to be of low cross-sectional area. In this “low profile” condition, the mesh is placed in or on a catheter. The stent is then positioned at the site of the vascular region to be treated. Once in position, the wire mesh stent is released and allowed to expand to its desired cross-sectional area generally corresponding to the internal diameter of the vessel. Similar solid stents are also disclosed in U.S. Pat. No. 3,868,956 to Alfidi, et al. The metal stent functions as a permanent intra-vascular scaffold. By virtue of its material properties, the metal stent provides structural stability and direct mechanical support to endoluminal surfaces and the bulk of the vascular wall. Stents of the type described above are either balloon-expandable or resiliently self-expanding due to their helical “spring” geometry. Other stents have also been designed in recent years. Among these are stents formed from polymeric materials and stents formed from materials which exhibit shape memory.
The complications associated with permanent implants such as the coronary stents result from multiple factors including: (1) Issues related to the biocompatibility of the implant—local wall reaction, e.g. foreign body, inflammation, immune responses, wall tissue compression, specific material composition; (2) Alterations of blood flow resulting from the creation of flow disturbances due to protrusion of stent element in the blood flow field, as well as unusual geometries and topographies; (3) Underlying tissue, e.g. vessel wall issues and disease; and/or (4) Inherent design deficiencies in the stenting devices. The stent is a foreign object (i.e., not native to the body); it incites a thrombotic, inflammatory, local tissue reaction, and an immune response. This may cause cell activation, migration and proliferation to rapidly occur over the stent—termed “neointimal thickening” or “hyperplasia”. In addition, there is a strong tendency for clots to form at the site where the stent damages the arterial wall. The size and/or structure of the stent may give rise to mechanical stability problems. Recent studies measuring the relative radial compressive stiffness of known wire stents, as compared to physiologically pressurized arteries, have found the stents to be much stiffer than biological tissue. These studies lend support to the concept of poor mechanical biocompatibility of many currently available stents. The permanent placement of a non-retrievable, non-degradable, foreign body in a vessel to combat restenosis, which is predominately limited to the six-month time period post-angioplasty, is another major drawback of coronary stenting, i.e., a temporal mismatch. Furthermore, typically the coronary stent is a purely structural element; it is not responsive and does not monitor changes in arterial function, i.e. does not monitor blood flow rates and/or the presence of an immune response to the stent.
It is therefore an object of this invention to provide materials and/or methods for forming smart biomedical implants on endoluminal surfaces without the need for invasive medical procedures.
It is a further object of this invention to provide improved materials and/or methods for forming smart biomedical implants on endoluminal surfaces that are biodegradable over the useful lifetime of the implant.
It is a further object of this invention to provide improved smart biomedical implants and systems for forming smart biomedical implants that are biodegradable in a controlled manner.
It is a further object of this inventions to provide improved materials and/or methods for forming smart biomedical implants on endoluminal surfaces that have integrated electronic devices that can locally monitor and/or modify the function of an organ or organ component.